Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alport's syndrome is a hereditary disease striking cochlea, eye and kidney. The diseased women usually have a nonlethal degree of the kidney disease, but the prognosis for the men is worse. They often die from renal failure before the age of 35. Most cases of hearing loss occurs in men. The hearing loss is progressive after the age of 10. Audiological tests are characteristic for a cochlear lesion. The debut of the disease usually appears in the post natal period giving microscopic haematuria. It can, however, occur later with haematuria and proteinuria. The hearing loss may be the first symptom, which is an observandum to otologists. Two families with Alport's syndrome are described. The patients have been examined concerning kidney disease, audiological and vestibular pathology. The hereditary pattern is described.
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PMID:Two families with Alport's syndrome. 98 81

A retrospective record analysis of 112 juvenile-onset diabetics with nephropathy was conducted in order to determine their clinical course. The mean duration of diabetes at the onset of proteinuria was 17.3+/-6.0 years. Early renal failure appeared two years after the onset of protein-uria, and severe renal failure (mean serum creatinine level, 8.5+/-3.9 mg/100 ml) four years after the onset of proteinuria. The mean duration of life after the onset of severe renal failure was six months. The mortality was 53%, with 59% of the deaths attributable to renal failure and 36% to cardiovascular disease. All patients experienced progressive deterioration of renal function as well as the other complications of diabetes, the rate of progression being accelerated toward the end of the course. Juvenile onset diabetics should be considered for renal transplantation before the serum creatinine level reaches 8.5 mg/100 ml.
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PMID:The clinical course of diabetic nephropathy. 98 37

Renal biopsies of 23 heroin addicts who presented with the nephrotic syndrome were examined by light and electron microscopy. The majority of patients (14) showed focal segmental glomerular sclerosis on light microscopy, four patients showed "minimal change", and two were classified as "focal global sclerosis." In one case focal mesangial proliferation was the outstanding feature; one patient had diabetic glomerulosclerosis; and one had mesangiocapillary glomerulonephritis and dysproteinemia. Visceral epithelial swelling and proliferation were present in 14 patients on light on light microscopy. Electron microscopy showed distinct podocyte changes consisting of loss of foot processes, vacuolization, and cytoplasmic degeneration; focal separation of podocytes from basement membranes was found in 11 of 18 cases. In some instances a few electron-dense deposits were present in the mesangium. Membranous nephropathy was not encountered, although it occurs in 30 to 40% of unselected adult nephrotic individuals. Of 15 patients followed for 2 months to 5 years, one died of heroin overdose, eight went into renal failure, two improved, and four continued to have proteinuria. It is concluded that nephrotic syndrome of heroin addicts is most often associated with focal segmental glomerular sclerosis and occasionally with minimal change disease or focal global sclerosis. Conceivably these three conditions represent different phases of one disease process, although different reactions to heroin or its various vehicles and contaminants cannot be excluded. The morphologic resemblance to experimental aminonucleoside and N,N'-diacetylbenzidine-induced nephrosis suggests a possible toxic origin.
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PMID:Glomerular morphology in nephrotic heroin addicts. 99 59

The case is presented of a young man who, after prolonged intravenous narcotic administration, developed subacute bacterial endocarditis involving the aortic valve, and rapidly progressive glomerulonephritis. After treatment of and recovery from renal failure, persistent proteinuria was shown to be caused by focal glomerulosclerosis. The association of these lesions with "mainlining" is reviewed.
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PMID:Renal and cardiac complications of drug abuse. 99 44

The defect in glomerular permeability that leads to proteinuria can be assessed by determining the relative clearance of macromolecules of known but different dimensions, that is, glomerular selectivity. Such estimates can be made using naturally occurring plasma proteins and dextran or polyvinylpyrrolidone injected into the circulation. In preeclampsia, protein and dextran selectivities show good concordance. The proteinuria is intermediate in its selectivity. These findings confirm that proteinuria is glomerular in origin and that the glomerular abnormality is uniform throughout the majority of functioning glomeruli. In abruptio, protein selectivity is very low and dextran selectivity is high. This pattern is seen also in acute ischemic renal failure and suggests that the true glomerular functional defect is actually less severe than in preeclampsia and that much of the protein in the urine in abruptio is postglomerular in origin. The structural lesion in preeclampsia is "characteristic" only in the sense that a number of individual components of glomerular injury, which are themselves commonly seen in other glomerular disorders, occur in a particular balance, and not because of any single unique or specific feature. The important components--that is, endothelial swelling, mesangial cytoplasmic activity, subendothelial deposits, and occational thrombosis of the afferent arterioles--all occur, albeit to a lesser degree, in abruptio placentae, as well as in other glomerular disorders in which intravascular coagulation is a primary cause or plays a major role.
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PMID:Proteinuria and the renal lesion in preeclampsia and abruptio placentae. 100 54

Radiological findings of segmental renal hypoplasia are reported, based on the observation of 6 children aged between 8 and 14. The leading clinical symptom is arterial hypertension. Urinary tract infection and proteinuria are additional common findings. Cases with bilateral disease often have renal failure. The intravenous urogram shows unilateral or bilateral small kidneys with segmental renal scarring and transverse lobulation. In the pathological areas the calyces are ectatic or clubbed and their infundibulum is elongated. Vesico-ureteral reflux is frequent. In angiography the lobulated segments appear hypovascular. Diagnosis was verified by histological examination.
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PMID:Segmental renal hypoplasia in childhood. 101 4

This paper reports on a 26 year old male who died of toxic diphtheria with all typical features such as: Bullneck, paralysis of the soft palate, renal failure accompanied by proteinuria and--most notably--myocarditis (very typical microscopically) with circulatory disturbances and finally left and right hand failure. The myocarditis hat caused increases of SGOT, SGPT, CPK, LDH and HBDH to values not seen before by us in the course of myocarditis. The patient had been immunized against diphtheria as a child. Initial treatment consisted of the application of ampicillin which caused rapid regression of the local symptoms in the pharyngeal region including the bullneck-symptom; of course the course of intoxication was not influenced, even after the patient had been admitted to the hospital, the disease correctly diagnosed and antitoxin given three days before death.
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PMID:[Fatal diphtheria in a 26-year-old man. Repetitorium; Known and current aspects of diphtheria]. 101 48

The manifestations, clinical course and treatment of 14 patients with non-malignant renal vein thrombosis are described. Most patients (10 of 14) had generalized vague illness and nephrotic syndrome but 4 were initially seen with acute symptoms of flank pain, hematuria or hypertension. Renal vein thrombosis affected young men 2.5 times more often than women and occurred on the left side 2.6 times more commonly than on the right or both sides. Red blood cell casts in the urinary sediment, heavy proteinuria and hypoalbuminemia were useful indicators of the disease. Excretory urographic signs were suggestive of renal vein thrombosis in all patients and these were corroborated by angiographic studies. Systemic anticoagulation with or without a renal failure program and diuretics, or simply a combination of the last 2 modalities, was used in 9 patients. In 2 of the 9 patients who were unresponsive the adjuvant use of cyclophosphamide and steroids effected a cure. The remaining 5 patients underwent nephrectomy or thrombectomy. All 14 patients were followed for 1 to 7 years (mean 1.6 years). Ten patients were cured or improved, 1 patient was unchanged, and in the remaining 3 patients the condition deteriorated and they subsequently required a renal allograft. The rationale for various forms of treatment is discussed.
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PMID:Renal vein thrombosis. 105 24

Forty cases of focal sclerosing glomerulonephropathy with nephrotic syndrome or proteinuria were studied retrospectively in regard to clinical presentation, response to steroid therapy and clinical course, and histopathology of the lesion. Morphologically there was a focal segmental and global sclerosis with subendothelial hyaline deposits, collapse of the capillary loops, intracapillary hyaline material or foam cells, filling and widening of the mesangium with mesangial matrix, focal tubular atrophy, and focal interstitial fibrosis. Thirty-four patients had been treated with prednisone; initial complete remission of the nephrotic syndrome occurred in only 4 patients and partial remission in 10. Nine of these 14 patients had nephrotic relapse or became resistant to steroids. Thirty-three percent of the patients progressed to end-stage renal failure and an additional 25 percent had impairment of renal function after a mean of 8 years from onset. Three patients received kidney allografts, and in two the disease recurred in the transplanted kidney. Focal sclerosing glomerulonephropathy associated with nephrotic syndrome or proteinuria appears to be a clinicopathologic entity characterized by resistance to steroid treatment, frequent progression to end-stage renal disease, and recurrence in the transplanted kidney.
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PMID:Focal sclerosing glomerulonephropathy: a clinicopathologic study. 109 Jul 90

Described here are the findings of a clinical, anatomic and chemical study of 40 patients having an original lesion of the basement membranes of the kidney. This lesion is characterized by an ultrastructural modification of the basement membrane substance which appears very dark (black) and homogeneous in electron micrographs. It affects the basement membranes of the glomerulus, Bowman's capsule and the renal tubules. Patients with this lesion all manifest the clinical course of a chronic enphritis and is almost invariably accompanied by proteinuria and microscopic hematuria. The disease evolves generally with intermittent episodes towards irreversible renal failure. Eight patients received kidney transplants. Study of these transplants has shown that the lesion recurs in the transplanted kidneys during the year following transplantation. Moreover, it is never found in kidneys transplanted into patients who did not have it in their own kidneys. This ultrastructural lesion can therefore be placed in the framework of a systemic disease whose etiology is not yet known. The study of these transplants also shows that the lesion can exist despite the absence of any detectable clinical or biologic signs and be well tolerated for periods which now exceed 4 years for three patients.
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PMID:Electron dense alteration of kidney basement membranes. A renal lesion specific of a systemic disease. 109 27


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